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M A Boim

Publications and source records attributed to M A Boim.

45 records · Page 3Linked to original sources
PubMed1986

Renal haemodynamics in spontaneously hypertensive rats with superficial glomeruli.

Spontaneously hypertensive rats (SHR) were mated with Munich-Wistar rats (MW), and the F1 hybrids were called Escola Paulista de Medicina (EPM) rats. The EPM rats present spontaneous hypertension and superficial glomeruli, allowing a study of glomerular haemodynamics. Mean whole kidney (GFR) and single nephron glomerular filtration rate (SNGFR), and mean total and glomerular plasma flow, were similar in EPM and MW rats. However, a higher glomerular capillary hydraulic pressure and a reduced ultrafiltration coefficient (Kf) of EPM rats were observed. The glomerular hypertension may be the cause of low Kf, a possible initial lesion of glomerular sclerosis. When mean arterial pressure levels were reduced to about 90 mmHg, a maintenance of SNGFR, with a 40% reduction in GFR, in EPM rats were achieved, suggesting an autoregulatory mechanism in the superficial but not in the juxtamedullary nephrons. The decrease on urinary sodium excretion (UNaV) in this condition, which was also lower than in MW rats, showed an impaired sodium handling by EPM kidneys, a possible role in the hypertension genesis. Thus, the data suggest that EPM rats can be a useful model for glomerular haemodynamics and microcirculatory studies in the spontaneously hypertensive state.

Animals↗
PubMed1985

Role of the prostaglandin and kallikrein-kinin systems in aminoglycoside-induced acute renal failure.

The role of humoral factors in the pathogenesis of gentamicin and tobramycin aminoglycoside-induced acute renal failure was studied in rats. Renal function was evaluated after inhibition of prostaglandin synthesis with indomethacin and inhibition of the kallikrein-kinin system with aprotinin. Plasma and urinary kallikrein levels were measured in aminoglycoside-treated rats, as was in vitro effect of of these antibiotics on plasma kallikrein activity and prekallikrein activation by dextran sulfate. Indomethacin treatment (2 mg kg-1 day-1, ip, for 13 days) of rats which received gentamicin or tobramycin (40 mg kg-1 day-1, ip, for 10 days) caused a further fall in glomerular filtration rate (GFR) and renal blood flow and an impressive increase in renal resistance. The effect of indomethacin on GFR was more evident for gentamicin- than tobramycin-treated animals. Aprotinin administration had no additional effects on the renal function of antibiotic-treated rats. Plasma and urinary kallikrein levels in aminoglycoside-treated rats were significantly lower than in untreated controls. Both aminoglycosides at concentrations of 0.1 mg/ml inhibited dextran sulfate activation of plasma prekallikrein, and 2.0 micrograms/ml tobramycin, but not gentamicin, inhibited the hydrolysis of H-D-Pro-Phe-Arg-p-nitroanilide by rat plasma. These data suggest that prostaglandins may protect against aminoglycoside nephrotoxicity.

Acute Kidney Injury↗
PubMedDate not supplied

Renal hemodynamic response to erythropoietin-induced polycythemia in 5/6 nephrectomised rats is different from normal rats.

The effects of recombinant human erythropoietin (rHuEPO)-induced polycythemia on renal function and glomerular hemodynamics were evaluated in Munich-Wistar rats (MW+EPO) before and after infusion of indomethacin; the rHuEPO effects on total renal function were also evaluated in 5/6 nephrectomized (CRF) MW and spontaneously hypertensive rats (MW-CRF+EPO and SHR-CRF+EPO, respectively). In normal MW rats, rHuEPO (300 IU/kg BW, 3 x /week, during 2 weeks) induced elevation in MAP, with maintenance of GFR, paralleled by superficial vasodilatation and elevation in SNGFR, suggesting cortical blood redistribution. These hemodynamic alterations induced by rHuEPO were blunted by indomethacin, suggesting a participation of the vasodilator prostaglandins in the renal compensatory mechanism of polycythemia. Elevation in MAP and reduction in GFR occurred in the MW-CRF+EPO group compared with the group receiving vehicle. In contrast, the SHR-CRF+EPO presented a reduction in MAP and maintenance of GFR, suggesting different rHuEPO effects depending on previous renal function and/or hypertensive state.

Animals↗
PubMedDate not supplied

[Kidney glomerular hemodynamics in the rodent Calomys callosus].

Renal function was characterized in Calomys callosus, a rodent which can participate in the transmission of several human diseases. The results showed that the pressures levels, hematocrit and plasmatic proteins were similar to rats submitted to the same experimental maneuvers. The corporal and renal weights, whole and single nephron glomerular filtration rates were similar to the mouse. This rodent presented a significant number of superficial glomeruli, allowing to evaluate glomerular hemodynamics and renal microcirculation parameters. Despite mean arterial pressure similar to the Munich-Wistar (MW) rats, mean glomerular capillary hydraulic pressure was lower in Calomys callosus, due to a lower post glomerular resistance in this rodent when compared to MW rats. The mean glomerular plasma flow rate was relatively elevated when compared with single nephron glomerular filtration rate, which in turn blunted the lower intraglomerular hydraulic pressure, and thus increased the single nephron glomerular filtration rate per g/kidney. The present work suggests that despite of the technical difficulties imposed by the reduced size of the Calomys callosus, the study of the renal function and glomerular hemodynamics is possible, establishing therefore, a model for the study such renal function.

Animals↗
PubMedDate not supplied

Effect of the antiglucocorticoid RU-486 on glomerular hemodynamics in remnant nephrons.

Endogenous glucocorticoid (GC) has been proposed to play a role in the adaptive functions of remnant nephron and participates in the progression of renal disease. The effect of GC blockade by RU-486 (20 mg/kg), an anti-GC agent, on the progression of chronic renal failure (CRF) was evaluated in Munich-Wistar rats. CRF was induced by 5/6 nephrectomy. Global renal function, glomerular hemodynamics, proteinuria and renal histopathology studies were performed after 60 days of CRF induction. RU administration in control or CRF groups did not induce significant changes in total renal function, mean arterial or intraglomerular hydraulic pressures, 24-hour proteinuria or sclerosis index. However, RU induced a significant reduction in single-nephron glomerular filtration rate in the superficial nephrons in both groups' control (decreases 20%) and CRF (decreases 57%), without changing total glomerular filtration rate, when compared with vehicle administration. These reductions were due to a decline in glomerular plasma flow rate (QA) and in glomerular ultrafiltration coefficient (Kf). These data suggest that GC played a role in the adaptive hyperfiltration associated with the compensatory mechanism but did not participate in the genesis of proteinuria or glomerulosclerosis in this experimental model.

Animals↗